Asthma affects over 150 million individuals and is clinically diagnosed by a barrage of symptoms, which include wheezing, coughing, and shortness of breath (Akinbami 2011; Miller 2001). Asthma can be subcategorized into two classes: allergic, and non-allergic asthma, which constitute roughly 70% and 30% of cases, respectively. Although there are almost no observable differences in the types of physiological changes that occur between the two subcategories, non-allergic asthmatics incur more severe and more frequent symptoms (Romanet-Manent 2002).
Airways of asthmatic individuals are distinguished through structural modifications, collectively called airway remodeling that includes bronchiolar inflammation, epithelial sloughing, goblet cell metaplasia, multiplied mucus glands, thickening of the lamina reticularis, increased airway smooth muscle mass, angiogenesis, and alterations in the extracellular matrix components (Fireman 2003; Hyde 2006). Additionally, B lymphocytes, T lymphocytes, eosinophils, neutrophils, and macrophages also migrate to the airways, triggering the release of immunoglobulin E, leukotrienes, prostaglandins, histamines, and other chemical mediators leading to airway inflammation (Bradley 1991; Henderson 1996).
In asthmatic individuals, T cells differentiate preferentially towards type 2 helper T cells (Th2) (Harrington 2005). Th2 cells are thought to induce asthma through the secretion of many cytokines that activate inflammatory pathways both directly and indirectly (Zimmermann 2003). Notably, Th2 cells secrete IL-13 which triggers STATE activation through activation of surface receptors present on eosinophils, mast cells, B lymphocytes, fibroblasts, and airway smooth muscle cells IIs (Chatila 2004, Akdis 2011, Jiang 2000, Cohn 2004, Medoff 2008). This activation leads to IgE synthesis, mucus hypersecretion, airway hyperreactivity, and tissue fibrosis (Munitz 2008). Overexpression of IL-13 is necessary and sufficient to induce non-allergic asthma (Munitz 2008; Akdis 2011; Wills-Karp 1998).
There is a need to identify improved markers for lung inflammation. There is also a need for methods of detecting asthma and differentiating between allergic and non-allergic asthma.